Assistant Professor of Biology
Office: Baker-Hebron 13
I am committed to helping students become scientists in daily life. A student scientist seeks knowledge open-mindedly, analyzes information critically, solves problems creatively, and communicates conclusions effectively. These are skills that we learn in class and apply throughout our lives.
Through my own enthusiasm for biology, I encourage students to find topics that lead them to further inquiry, from non-majors fulfilling general education requirements to upperclassmen pursuing independent studies.
I believe UIU stands out through its diversity of student studies. As a member of the biology department, my goal is to prepare you for wide variety of paths on the whole scale of biology, from the cell to the biosphere. Whether your plan is to study disease at the level of our cells and genes, the workings of an athlete's body, the population ecology of a herd of deer, the health of an agricultural field, or the conservation of our natural resources, you will find a path of study at UIU that excites your interests and prepares you for next step.
- Principles of Biology I
- General Biology
- Cell & Molecular Biology
- Cancer Biology
- Microbial Ecology (future)
B.A. in Biology from Lawrence University, Appleton, WI
Ph.D. in Biomedical Studies--Cell Biology and Genetics from Mayo Clinic Graduate School, Rochester, MN
Post-Doctoral Studies in Microbiology/Immunology at National Jewish Health, Denver CO
- 2012-present Member, American Society of Microbiology
- 2011-present Associate Faculty Member, Faculty of 1000
- 2011-present Peer Reviewer, Public Library of Science One (PLOS One)
- 2005-present Member, American Society of Cell Biology
I am interested in how bacteria use weapons to defend themselves from other organisms and to attack other species. I study Listeria monocytogenes, bacteria that is normally found in the soil but which causes illness in humans when we eat contaminated foods. Listeria secretes the protein p60 as a weapon that can manipulate our immune response during an infection, and also attack the defensive cell walls of other bacteria.
My research studies focus on how this weapon, enzyme p60, can act against bacterial competitors that Listeria may encounter in the soil or against helpful probiotic bacteria found in fermented foods. These studies will help us learn more about bacterial communities in the environment, in our foods, and in our own bodies. We can also apply this research to ecological bioremediation and to improving food safety.
Examples of student projects
Characterize preferred p60 substrates
Enzymes that degrade bacterial cell walls are secreted by some bacteria to lyse competing neighbors. Such competition using lactic-acid producing bacteria (LAB) is an emerging strategy to inhibit Listeria growth in the food industry. The enzyme p60 is more efficient on certain types of cell walls, likely due to the various chemical modifications these organisms use to disguise their defense system. Student projects may characterize p60 enzymatic activity against cell walls from LAB strains or soil bacteria to identify p60-resistant species as effective industrial competitors against Listeria.
Evaluate how variations in the p60 active site influences activity
The p60 protein is related to a large family of homologous enzymes with the same basic structure. However, the active site, or "business end" of the enzymes in this family can vary, and these variations can alter the activity level of the enzymes when acting on cell wall substrates from different organisms. Student projects may compare the activity of p60 family members acting on specific substrates. Students may also do mutation studies to alter p60 activity, and connect the changes in activity to physical changes of the p60 active site.
Determine whether p60 gives a competitive advantage
If Listeria secretes p60 to antagonize other bacteria, then Listeria mutants lacking p60 expression should show reduced fitness against both natural environmental and potential LAB competitors. Student projects could include measuring Listeria fitness against microbial competitors such as soil species and LAB strains, in the presence or absence of p60 production.
Recent Publications and Presentations
- Schmidt, R. L. and Lenz, L.L. (2013) "Adjuvants Targeting the DNA Sensing Pathways– Cyclic-di-GMP and Other Cyclic-di-Nucleotides" chapter in DNA Sensing: The impact of dsDNA on Disease and Vaccinology ed. Ishi, K., and Tang, J.C.K. Elsevier.
- Schmidt, R.L. and Lenz, L.L. (2012) Distinct Licensing of IL-18 and IL-1β Secretion in Response to NLRP3 Inflammasome Activation. Public Library of Science ONE 7(9): e45186. Epub Sept 18.
- Williams, M.A., Schmidt, R.L., Lenz, L.L. (2012) Listeria monocytogenes interactions with the innate and adaptive immune system. Trends Immunol. Oct;33(10):488-95. doi: 10.1016/j.it.2012.04.007. Epub Jun 5.
- Schmidt, R.L. and Lenz, L.L. (Sept 2012) Listeria p60 Protein and Distinct NLRP3 Inflammasome Activation. Colorado Immunology Conference. Poster Presentation
- Schmidt, R.L. Filak, H.C., Lemon, J.D., and Lenz, L.L. (Dec 2011) The Listeria p60 Protein Co-opts the Inflammasome in Mature DCs to stimulate NK cell activation. American Society for Cell Biology Annual Meeting. Poster Presentation
- Schmidt, R.L., Filak, H.C., Lemon, J.D., Potter, T.A., Lenz, L.L. (2011) A LysM and SH3-domain containing region of the Listeria monocytogenes p60 protein stimulates accessory cells to promote activation of host NK cells. PLOS Pathogens 7(11): e1002368. Epub Nov 3.
- Schmidt, R.L., and Lenz, L.L. (Jan 2011) The Listeria p60 Protein Stimulates NK Cells by Activating the Inflammasome in Mature DCs. NK and NKT Cell Biology Keystone Symposium. Poster Presentation
- Schmidt, R.L., Rinaldo, F.R., Hesse, S.E., Hamada, M., Ortiz, Z., Beleford, D.T., Page-McCaw, A., Platt, J.L., Tang, A.H. (2011) Cleavage of PGRP-LC receptor in Drosophila IMD pathway in response to live bacterial infection in S2 cells. Self/Non-self;2(3). July/Aug/Sept (Accepted Jan 2009)
- Ahmed, A.U, Schmidt, R.L., Park C.H., Reed, N.R. Hesse, S.E., Thomas, C.F., Molina, J.R., Deschamps, C., Yang, P., Aubry, M.C., and Tang, A.H. (2008) Effect of Disrupting Seven In Absentia Homolog 2 (Drosophila) Expression on Lung Cancer Cell Growth. J.Natl. Cancer Inst. Nov 18;100:1606-1629.
- Schmidt, R.L, Park C.H., Ahmed, A.U., Reed, N.R., Gundelach, J.H, Knudsen, B.E., Tang, A.H. (Dec 2008) Inhibition of K-RAS-Mediated Tumorigenesis and Metastasis by Blocking SIAH E3 Ligase-Dependent Proteolysis in Pancreatic Cancer. American Society for Cell Biology Annual Meeting. Poster Presentation, featured in "Novel and Newsworthy" ASCB press release
- Schmidt, R.L. (Oct 2008) Putting on the Breaks: Inhibiting Ras-mediated Tumorigenesis. Lawrence University, Appleton, WI. Recent Advances in Biology Lecture Series. Oral Presentation
- Schmidt, R.L., Trejo, T.R., Plummer, T.B., Platt, J.L., Tang, A.H. (2008) Infection-induced proteolysis of PGRP-LC controls the IMD activation and melanization cascades in Drosophila. FASEB J. Mar;22(3):918-29. (Epub Oct 16, 2007)
- Schmidt, R.L., Ahmed, A., Park, C.H., Gundelach, J.H., Cheng S., Knudsen B. and Tang A.H. (2007) Inhibition of RAS-Mediated Tumorigenesis by Blocking the SIAH-E3 Ligase-Dependent Proteolysis. Cancer Res. Dec 15;67(24):11798-810.